Tag Archives: HFLC

20 July 2014 HIGH CARBS OR LOW CARBS? THE BIG FAT SURPRISE – which is best for weight loss? a collaborative literature metanalysis study July 2014 by Naude ea the universities of Stellenbosch, Cape Town and Liverpool (UK) claimed to compare the effects of low CHO and isoenergetic balanced weight loss diets in overweight and obese adults, stratified by outcomes at 3-6 months and 1-2 years. Of nineteen trials (n = 3209), 3 had adequate allocation concealment. In non-diabetic participants, analysis showed little or no difference in mean weight loss in the two groups at 3-6 months (MD 0.74 kg) or for blood pressure, LDL, HDL and total cholesterol, triglycerides and fasting blood glucose. In diabetic participants, findings showed a similar pattern. CONCLUSIONS: Trials show weight loss in the short-term irrespective of whether the diet is low CHO or balanced. There is probably little or no difference in weight loss and changes in cardiovascular risk factors up to two years of follow-up when overweight and obese adults, with or without type 2 diabetes, are randomised to low CHO diets and isoenergetic balanced weight loss diets.

‘But Noakes points out, Low-fat, high-carb, high-sugar diet a likely cause of obesity/diabetes “I refer to the report in the Cape Times of July 10, “Noakes’s popular low-carb diet is not healthier, better for weight loss – study “. Since the authors of that study (Naude ea) do not understand either what constitutes a low-carbohydrate diet or the unique biological effects of such diets, they were predisposed to produce a biased report that comes to exactly the wrong conclusion.

‘First, the conclusion of their study was predictable since the authors chose to review only studies in which subjects ate the same number of calories on both diets. It is not clear how the authors conceived that diets that provided exactly the same number of calories would produce different outcomes. Indeed, a core teaching of these nutritional scientists is that the degree of weight loss is determined by the reduction in calorie consumption. Thus the authors knew the outcome of their study even before they undertook it. This is not good science.

‘Second, the studies included in their meta-analysis are not of the low-carbohydrate diet described by either Dr Robert Atkins or ourselves in Real Meal Revolution. Dr Atkins realised in the 1970s that the majority of overweight/obese persons can only reduce their weights successfully, and keep that weight off in the long term, if they eat less than 60g carbohydrate/day for the rest of their lives. Higher intakes are increasingly less effective. In Real Meal Revolution we stress that those with insulin resistance/ type 2 diabetes need to keep their carbohydrate intakes even lower, ideally to about 25g/day. The “low-carbohydrate ” diets included in the meta-analysis provided a minimum of 200g carbohydrate/day (or 4-8 times higher than the carbohydrate content that is known to be effective). As a result this is a meta-analysis of studies providing a high, not a low-carbohydrate load for those with obesity/insulin resistance/type 2 diabetes.

‘Third, the extent of weight loss in the studies included in he meta-analysis is small, the greatest values being about 10kg. For most people with significant weight problems, such small weight losses are probably relatively meaningless and should be classified a diet failure, not a success. But freeliving persons who follow individually prescribed carbohydrate diets providing about 25g carbohydrate/day report quite remarkable degrees of weight loss, not infrequently up to 40-80kg, usually achieved effortlessly if the low-carbohydrate rules are followed.

‘Fourth, the unique biological effects of the properly-defined low-carbohydrate is that (i) It reduces hunger, allowing subjects to eat fewer calories without experiencing continual hunger. The point, as stressed by Dr Atkins, is that the low-carbohydrate diet is a low-calorie, no-hunger diet. (ii) The diet lowers blood insulin concentrations. In those with obesity/insulin resistance/metabolic syndrome, it is continually elevated blood insulin concentrations that cause ill-health (as clearly established by the work of Dr Gerald Reaven of Stanford University over the past 50 years).

‘The authors found that health benefits were no different on either diet. A number of properly designed, peer-reviewed meta-analyses of the real low-carbohydrate diets show that weight loss and health benefits are superior compared with higher-carbohydrate diets. Unfortunately, the authors appear to be ignorant of those studies since neither they nor your reporter refers to them. This implies the presence of bias, questioning the true intent of the report.

‘The report also includes the statement of the Heart Foundation of South Africa (HFSA) to the effect that a diet high in saturated fat causes heart disease. Unfortunately, the HFSA spokesperson appears unaware of Nina Teicholz’s recentbook, The Big Fat Surprise: Why Butter, Meat, Cheese Belong in Healthy Diet, and the June 23 Time Magazine Ending the War on Fat, which show that this dogma is false and is not based on any credible science. It is time the HFSA updated its understanding of what actually causes heart disease. They might also want to consider whether their promotion of their unproven low-fat, high-carbohydrate, high sugar diet for the past 37 years is the most likely direct cause of the obesity/diabetes epidemic that has since engulfed South Africans.

‘Indeed on a practical side, I wonder if the authors have ever considered studying the dietary intakes of the obese diabetic patients they treat at Tygerberg and Groote Schuur hospitals. Do patients with these diseases eat either high- or low-carbohydrate diets? Why is is that these twin diseases, which are crippling the health services of the Western Cape, began to increase exponentially only after the 1977 Dietary Guidelines that institutionalised the low-fat, high-carbohydrate diets? Surely these are the critical questions that should really be exercising the minds of the Western Cape’s nutritional scientists? The best conclusion that can be drawn from this study is that diets providing more than 10 percent of daily calories in the form of carbohydrate are equally ineffective in producing meaningful degrees of weight loss in those with obesity/insulin resistance/type 2 diabetes.”

already 30 years ago Seely and Horrobinin ‘Diet and breast cancer: possible connection with sugar consumption’ hypothesized: younger and older (possibly pre- and post-menopausal )women differ with respect to such correlations. In older women a strong correlation was found between breast cancer mortality and sugar consumption (correlation coefficient = 0.9).. In younger women the correlation with diet is weak. A possible connecting link between sugar consumption and breast cancer is insulin. This is an absolute requirement for the proliferation of normal mammary tissue and experimental mammary tumours may regress in its absence. Insulin secretion occurs in response to blood glucose level and could be excessive if the regulatory mechanism is overtaxed by large sugar intake. The same mechanism might account for the increased risk of mammary cancer in diabetics.

Hence the HighFat LowCarbs (William Banting 1863) diet is now established by the rigorous scientific references of the past 150 years assembled by science writer Gary Taubes in The Diet Delusion , and advised to all for prevention and management of obesity and all other common major diseases including breast and all cancers.

As investigative journalists write recently, like Taubes and rational scientists the past 50years, the major cause of all common chronic degenerative disease including cancer and immunoincompetence is not fat but refined carbs – the root cause of the SACCHARINE DISEASES that Cleave, Campbell, Burkitt reported occurring in pastoral tribes converting to the western commercialized diet of sugar, refined cereals and rice . They note that in the Mouse Cancer Study in cancer-prone mice,

Gemma Llaverias ea, Jefferson University, Philadelphia 2011, which claimed that high (fat)cholesterol intake promotes breast cancer, the control mice (not major carnivores but omnivores) were fed a balanced natural chow with 4.5% fat, 23% protein, and 50% carbohydrate, whereas the test mice were fed a totally synthetic chow meant to represent a western human cholesterolemic diet: 20% fat, 17% protein, and 48% carbohydrate. So in fact the high risk factor for cancer and all disease was not the higher fat intake (20% as dairy fat) vs 4.5%- from fish meal and soy/cereals) but the 48% carbs (2/3 sucrose, 15% (malto)dextrins -which absorb as rapidly as glucose) intake and 19% casein (a major health problem) in the test chow. They failed to include a control group on what is natural mouse diet ie free of refined carbs and milk : “RSPCA 2014: Wild mice – opportunistic omnivores- will eat a wide variety of seeds, grains, and other plant material as well as invertebrates, small vertebrates and carrion“. Thus plenty of natural seed/grain fats and mixed protein and plant carbs, zero sugar or refined carbs- ie the Banting diet. ..

A new 18year observational followup study from Swedenlast year in 62000 people assessed total energy intake – carbohydrate from median 61 to 39% , protein 11 to 19% , and fat 27 to 42% . LCHP scores were positively related to intake of animal protein, but negatively related to plant protein. For carbohydrate and fat, associations were consistent in sucrose and whole grain and saturated and unsaturated fat, respectively. Across the range of macronutrients, there was no clear significant trend for particular cancers. This is not surprising as the intake of carbs ranged from 40 to 60% and fat from 27 to 42%. Thus no cohort was on a highfat low carbs ketogenic diet as Banting, Noakes et al find successful. . the lowest % carbs group at best had similar fat % intake ie there was no low-carbs cohort taking below 30% carbs..There is a vast difference in calorie intake between their “optimal’ LCHP 42:40 fat:carbs ie 1:1 , versus the true ketogenic HifatLowcarbs diet of eg 50:<30 fat:carbs ie >1.66:1.

The truth of more than four decades worth of research is now very clear: the potential benefit of mammography screening is small and the harms are substantial at all ages, but especially so for women in their 40s.

The bottom line is that mammography screening, implemented to reduce breast cancer deaths due to earlier detection of breast cancer, has been eclipsed by therapy and increased awareness.

The truth of more than four decades worth of research is now very clear: the potential benefit of mammography screening is small and the harms are substantial at all ages, but especially so for women in their 40s.

The bottom line is that mammography screening, implemented to reduce breast cancer deaths due to earlier detection of breast cancer, has been eclipsed by therapy and increased awareness.

A 49-year-old man presented to hospital with severe orthostatic hypotension, gingival dysplasia and a purpuric rash involving his extremities. The orthostatic hypotension failed to respond to fluids and, on the basis of physical examination and dietary history, the patient was given a preliminary diagnosis of scurvy (ascorbic acid deficiency). Serum ascorbicacid levels were undetectable and the orthostasis resolved within 24 h of ascorbicacid replacement. The pathogenesis of orthostatic hypotension in the setting of scurvy appears to involve impaired catecholamine synthesis and attenuated vasomotor response to α-adrenergic stimulation. We believe that this case describes a rare presentation of scurvy and highlights a previously under-reported connection between scurvy and vasomotor instability.

Br J Community Nurs. 2013 Suppl:S6, S8-11.Vitamin C: a wound healing perspective. Moores J. Vitamin C, also known as ascorbicacid (AA), is involved in all phases of wound healing. In the inflammatory phase it is required for neutrophil apoptosis and clearance. During the proliferative phase, AA contributes towards synthesis, maturation, secretion and degradation of collagen. Deficiencies affect the maturation phase by altering collagen production and scar formation. The body strives to maintain homeostasis of AA, thereby ensuring availability for collagen synthesis. After wounding, plasma and tissue levels of AA diminish and, as a consequence, supplements may be useful for healing, although levels beyond saturation are excreted. Clinicians need to be aware of both the nutritional status of patients with either acute or chronic wounds and the possibility of any AA deficiency which may hinder healing.

Nat Commun. 2013;4:1881. Mycobacterium tuberculosis is extraordinarily sensitive to killing by a vitamin C-induced Fenton reaction. Vilchèze C1,ea .Einstein College New York. Drugs that kill tuberculosis more quickly could shorten chemotherapy significantly. we show that vitamin C, a compound known to drive the Fenton reaction, sterilizes cultures of drug-susceptible and drug-resistant Mycobacterium tuberculosis, the causative agent of tuberculosis. While M. tuberculosis is highly susceptible to killing by vitamin C, other Gram-positive and Gram-negative pathogens are not. The bactericidal activity of vitamin C against M. tuberculosis is dependent on high ferrous ion levels and reactive oxygen species production, and causes a pleiotropic effect affecting several biological processes. This study enlightens the possible benefits of adding vitamin C to an anti-tuberculosis regimen and suggests that the development of drugs that generate high oxidative burst could be of great use in tuberculosis treatment.

VITAMIN D AND BREAST CANCER:

20 years agoNewmark from Sloan Kettering NY wrote : High dietary fat increases mammary epithelial cell proliferation, particularly the “hormonally driven” hyperproliferation during breast growth and development in young animals. Increased dietary calcium (and probably vitamin D) lessens the increase of proliferation induced by high fat. These data, although limited, suggest that the maximum effect of diet (high fat increase, as well as calcium and vitamin D modulation) on eventual breast cancer may be during puberty, and adolescence, when the mammary gland is actively growing and developing. (3) An inverse epidemiological correlation exists between sunlight availability as a source of vitamin D and the risk of breast cancer in the U.S. and Canada. (4) Current vitamin D and calcium dietary intake in the U.S. is far below the RDA in all female age groups, particularly for the elderly. (5) Reduction of breast cancer risk, and simultaneously osteoporosis, might be achieved by increasing dietary intake of calcium and vitamin D to RDA levels. This may be particularly applicable to females during puberty and adolescence.

It is likely that- given the limits on vitamin C intake due to diarrhoea, and cost, and bloating- increments in vit D3 intake well above the current mediocre antirachitic 400iu/d norm- up to the generally well-tolerated 10 000iu/day, (after a loading dose of 200 000 to 600 000iu). with supplement of vitamin K2- will give even better benefit against breast cancer than vitamin C.

IT IS COMMON CAUSE THAT ONE DOESNT, CANNOT PREVENT OR TREAT INFECTION BY POOR NUTRITION OR LOWDOSE ANTI- MICROBIALS- such policy is futile if not dangerous for breeding resistance as well as disease extension. The studies below confirm the obvious, (as Klenner, Pauling, Cameron ea showed the past 50 years with highdose vit C injection), that vitamin D3 orally also works as a multiantimicrobial agent if given as early as possible in safe very high dose and bloodlevel eg 600 000iu monthly (in the first month, – in Salhuddin’s Pakistan PTB patients (presumably also Sunni muslim) initially mean wt 45kg, thats vit D3 ~440iu/kg/d) for two doses ie a mean of 300iu/kg/day over 90days; not the current preventative recommendation of 80iu/kg /day to a safe blood level of around 50-60ng/ml. As Holick has said, with adequate water intake even 50 000iu vit D3 a day ie 1.5million iu/month for months causes no toxicity. Given the 40% mortality rate in the frail Saudi MERS patients, and in acute severe influenza and other serious viral infections, it can be expected that such highdose immediate vitamin D3 therapy orally with eg 600 000iu, combined with highdose vitamin C, zinc and some multivite, (never mind appropriate antibiotics in acute bacterial infection) will similarly virtually eliminate mortality.

But no KSA Govt website mentions this- except the Saudi Gazette a year ago which strongly urged vitamin D supplement in the KSA as even daily sun exposure does not bring most Saudi women above the vitamin D deficiency threshold. It says Since Muslim women can only reveal the hands and face, they may need to be out in the sun for longer than 30 minutes. But the review conspicuously fails to mention that in public outdoors in KSA, women must have even the head and face covered. It also propagates surprising dangerous nonsense that “severe deficiency needs monthly vitamin D injection – “Mom, have you taken your vitamin D injection this month?, when all it requires is an oral daily, weekly or fortnightly dose vitamin D3 at trivial cost.” It does stress “One of the main reasons why vitamin D deficiency is so common in the Kingdom is because there are very few food sources of vitamin D. Foods which have fairly good amounts of vitamin D are fish liver oil, sweet potatoes, egg yolks, vegetable oils, butter, and fatty fish such as salmon, sardines, and tuna,” said Dr. Rasha Jameel, a consultant in family medicine at a local hospital. In the United States, all milk and dairy products are fortified with vitamins A and D, but no such measures are in place in the Kingdom“.

This correlates with a new metaanalysis(in the BMJ this month) of observational studies from Europe and USA, that all-mortality hazard ratio over a mean of 10 years increases by 57% as vit D level falls from the highest to the lowest level. The KSA apparently chooses to ignore that, as this column reported recently from WHO data, despite apparently being the wealthiest country per capita of bigger populations in the world, KSA’s population life expectation is about 5 years lower than eg far less sunny Britain’s; ie KSA all-cause mortality rate is avoidably materially higher. Despite KSA medical professors having reported in studies that most of the KSA population is deficient in vits D and C, the KSA Govt website chooses to ignore this on official websites; unlike other even Middle-Eastern governments promoting vit D fortification or meaningful safe supplements costing trivial amounts.

Even a new study last year from KSA universitiesconfirmed that ” Most commonly consumed food products by Saudi population which are supposed to be fortified by vitamin D are either not fortified or contain an amount less than (apparently from their table 2 ~ half of) recommended by guidelines set for US marketplace”. Even a UAE authority recently stressed “Can fortified milk fight Vitamin D deficiency? Shockingly low levels of D3 among UAE population cannot be rectified by milk alone.” As Holick ea, including a Turkish University 2010 trial report, oral vitamin D3 is far more effective , and safer than, either vitamin D2, or vitamin D injection -never mind much cheaper. This current ostrich-head-in-the-sand denialism by the KSA government is like that of the RSA govt under Presidents Mbeki and Zuma 10-15 years ago about preventing and treating HIV-AIDS – considering that the safe and beneficial daily intake of vitamin D3 is now universally recognized as 4000 if not 10 000iu/day (ie about 80iu/kg/day or pro rata up to perhaps fortnightly) , to a mean blood vit D level of about 60 to 80ng/ml. .

As Prof Mike Holick pointed out a few years ago, “Even in Saudi Arabia, Qatar and South Africa, more than 50% of the population is deficient in vitamin D, all because of their avoidance of sun. Based on some of the literature, it seems that we could probably decrease health care costs across the board by 25% if everybody had optimal vitamin D status.” As Al Faraj ea reported in Riyadh in 2003, Prof Zahid Naeemfrom a KSA university wrote in 2010, “Vitamin D deficiency is an ignored epidemic in KSA and globally“; confirmed by a KSA study by Ali ea in 2012: “Even in a sunny country like Saudi Arabia the prevalence of vitamin D deficiency in young female is high“.. One does not need to speculate why the KSA and all governments globally choose to ignore this inconvenient truth, downplay effective vigorous vitamin C and D3 (sunshine) supplements- such widespread vitamin D and C deficiencies, like cigarette smoking and alcohol abuse, suit governments and Big Pharma- the Disease Industry- in reducing populations growths and creating jobs for the highly profitable Disease Industry and it’s shareholders- for whom Only Disease Pays. Cheap safe natural Prevention Does not Pay since it at least halves sickness never mind disease industry jobs, taxes and profiteering in the global $multitrillion Disease and Diet and Vaccine and Invasive Screening Industry scams.

As Salahuddin ea note, the good results in Pakistan in only 3 months with vigorous INITIAL dose vit D3 contrasts with Two recently published large randomised, controlled trials of conservative vitamin D3 over months that achieved far lower blood vitamin D levels found no difference in clinical outcomes or mortality after 400,000IU of 25-hydroxyvitamin D3 or placebo were given by Martineau ea in London, UK to 146 pulmonary TB patients – where mean (trough or midpoint) vit D level (after 100 000iu vitamin D(3) or placebo at baseline and 14, 28, and 42 days after starting standard tuberculosis treatment) – was surprisingly only 40ng/ml at 56days – ie after a mean of 7000iu/d by 56 days, vs 10ng/ml on placebo)- less than half of the bloodlevel achieved on vit D3 in the Pakistan trial ;

and by Wejse et al 2009 in Guinea-Bissau to 365TB patients – who received 300,000 IUs of vit D3 ie only 100,000 IU or placebo at inclusion and again 5 and 8 months after the start of treatment, ie below 1000iu vit D3 per day over the 12 month trial period “. The Guinea-Bisseau pts thus might have achieved a mean blood vit D level boost of only 10ng/ml.. and now Havers ea (Baltimore)show Low 25(OH)D is common in diverse HIV-infected populations and is an independent risk factor for clinical and virologic failure; Low 25(OH)D was associated with high body mass index (BMI), winter/spring season, country-race group, and lower viral load. Baseline low 25(OH)D was associated with increased risk of human immunodeficiency virus (HIV) progression and death (adjusted hazard ratio (aHR) 2.13; 95% confidence interval [CI], 1.09–4.18) and virologic failure (aHR 2.42; 95% CI, 1.33–4.41). and Shepherd ea (Eurocoord) Low Vitamin D predicts short term mortality in HIV-positive personsOdds of death decreased by 46.0%( P = .04) for a 2-fold increase in latest 25(OH)D level.. In patients with current 25(OH)D <10 ng/mL, hsIL-6 concentration increased by 4.7%(95% CI, .2,9.4, P = .04) annually after adjustment for immunological/inflammatory markers, and no change in hsCRP rate was observed (P = .76)